Abstract Alzheimer's disease (AD), characterized by the β-amyloid protein (Aβ) deposition
and tau hyperphosphorylation, is the most common dementia with uncertain etiology. The …

Background Synapse damage and loss are fundamental to the pathophysiology of
Alzheimer's disease (AD) and lead to reduced cognitive function. The goal of this review is to …

β-amyloid (Aβ)–dependent neuronal hyperactivity is believed to contribute to the circuit
dysfunction that characterizes the early stages of Alzheimer's disease (AD). Although …

It is increasingly accepted that early cognitive impairment in Alzheimer's disease results in
considerable part from synaptic dysfunction caused by the accumulation of a range of …

During recent years, the preclinical stage of Alzheimer's disease (AD) has become a major
focus of research. Continued failures in clinical trials and the realization that early …

Human Alzheimer's disease (AD) brains and transgenic AD mouse models manifest
hyperexcitability. This aberrant electrical activity is caused by synaptic dysfunction that …

Gamma oscillations (∼ 25–100 Hz) are believed to play a role in cognition. Accordingly,
aberrant gamma oscillations have been observed in several cognitive disorders, including …

Synapses are the site for brain communication where information is transmitted between
neurons and stored for memory formation. Synaptic degeneration is a global and early …

Neurodegenerative diseases are an enormous public health problem, affecting tens of
millions of people worldwide. Nearly all of these diseases are characterized by …

Mutations in β-amyloid (Aβ) precursor protein (APP) cause familial Alzheimer's disease (AD)
probably by enhancing Aβ peptides production from APP. An antibody targeting Aβ …